RETROVIRAL ENV-MEDIATED LEUKEMOGENESIS (MEETING ABSTRACT)

Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.

RETROVIRAL ENV-MEDIATED LEUKEMOGENESIS (MEETING ABSTRACT)

Fifteenth Symposium of the International Association for Comparative Research on Leukemia and Related Diseases. October 6-11, 1991, Padova/Venice, Italy, p. 3, 1991.. Unique Identifier : AIDSLINE ICDB/92682362
Amanuma H; Watanabe N; Ikawa Y; Tsukuba Life Science Center, RIKEN, Tsukuba, Ibaraki 305, Japan

Abstract: Friend spleen focus-forming virus (SFFV), originally isolated as one of the components of the Friend virus complex, is a member of the murine replication-defective type C retroviruses and induces acute, progressive erythroleukemia, called Friend disease, in adult mice. In the early stage, enhanced polyclonal proliferation of the erythroid progenitor cells occurs in the spleen of the infected mouse. The glycoprotein (gp55) encoded by the defective env gene of SFFV is responsible for this polyclonal proliferation. This gp55 gene alone induces the disease in transgenic mice. gp55 was reported to bind Epo-receptor to support IL-3-dependent cell growth, and especially sends signals dependent on this receptor. We performed extensive mutational analyses on the primary structure-biochemical property and biological activity relationship of gp55 in the polycythemia-inducing strain of SFFV using in vitro constructed mutants and the revertants isolated in vivo after the pathogenic selection. When the intracytoplasmic tail of gp55 is longer than 10 amino acids, the modified gp55 molecules cannot be released from the cells, and the reconstructed SFFV variants become nonleukemogenic. We present the results of these studies and discuss the mechanism of action of gp55 in the modulation of the function of the erythropoietin receptor. Recently, a murine Mink cell-focusing virus, env, was found to send signals to the IL-2 receptor (LI, J-P et al, personal communication) and UV-inactivated HTLV-1 particles showed mitogenic function (Gazzolo L et al, personal communication). These studies may initiate retroviral env-mediated leukemogenesis. (5 Refs)

Keywords: Animal Cell Division Erythroid Progenitor Cells/CYTOLOGY Gene Products, env/*GENETICS HTLV-I/GENETICS Leukemia, Experimental/*GENETICS Mice Mice, Transgenic Mink Cell Focus-Inducing Viruses/GENETICS Mitogens Receptors, Cell Surface/METABOLISM Receptors, Interleukin-2/GENETICS Spleen Focus-Forming Viruses/*GENETICS ABSTRACT
920830
M9281113

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